Smoking status and endothelial function in Japanese men

It is established that smoking is a major risk factor of atherosclerosis. Endothelial dysfunction occurs in the initial step in the pathogenesis of atherosclerosis and plays a critical role in the development of atherosclerosis. The purpose of this study was to evaluate the association between smoking status and endothelial function in detail in men. We measured flow-mediated vasodilation (FMD) in 2209 Japanese men including 1181 men who had never smoked and 1028 current smokers. All of the participants were divided into five groups by smoking pack-years: never smoker group (= 0), light smoker group (> 0 to 10), moderate smoker group (> 10 to 20), heavy smoker group (> 20 to 30) and excessive smoker group (> 30). FMD significantly decreased in relation to pack-years (6.6 ± 3.4% in the never smoker group, 6.8 ± 3.0% in the light smoker group, 6.5 ± 2.9% in the moderate smoker group, 5.9 ± 2.9% in the heavy smoker group, and 4.9 ± 2.7% in the excessive smoker group; P < 0.001). After adjustment for age (≥ 65 years), body mass index, systolic blood pressure, low-density lipoprotein cholesterol, glucose, and year of recruitment, FMD was significantly smaller in the excessive smoker group than in the never smoker group as a reference group (OR 1.95, 95% CI 1.42 to 2.67; P < 0.001). These findings suggest that FMD decreases with an increase in the number of cigarettes smoked and that excessive smoking is associated with endothelial dysfunction. Cigarette smoking is harmful to vascular function in men who are heavy smokers.

Optimal Campaign in the Smoking Dynamics

We present the optimal campaigns in the smoking dynamics. Assuming that the giving up smoking model is described by the simplified (potential-light-smoker-quit smoker) model, we consider two possible control variables in the form of education and treatment campaigns oriented to decrease the attitude towards smoking. In order to do this we minimize the number of light (occasional) and persistent smokers and maximize the number of quit smokers in a community. We first show the existence of an optimal control for the control problem and then derive the optimality system by using the Pontryagin maximum principle. Finally numerical results of real epidemic are presented to show the applicability and efficiency of this approach.

Clinical predictive factors for mutations in epidermal growth factor receptor (EGFR) exon 19 and 21 in Japanese patients with lung cancer

18131 Background: It has been reported that lung cancer with activating mutations of EGFR are highly sensitive to gefitinib or erlotinib. Furthermore, the incidence of EGFR mutations is significantly higher in adenocarcinoma, female, never-smoker, Japanese patients. However, it is difficult to take sufficient amount of biopsy specimen of lung cancer with advanced disease for mutation analyses in clinical practice. Therefore, in this study, clinical predictive factors for EGFR mutations in Japanese patients with lung cancer were clarified. Methods: EGFR exon 19 and 21 mutation status was determined in 284 tumor samples using direct sequencing, polymerase chain reaction. To identify clinical independent predictive factors for EGFR mutation, the logistic regression analysis was performed. Results: 131 tumors of them could be analyzed for mutations in EGFR exon 19 and 21. EGFR mutations were detected in 38 tumors (29%). Median age of patients with EGFR mutations was 62 years (rage 43–84); 19 male and 19 female; 18 stage I, 15 stage II, and 5 stage III disease. Cigarette- smoking history of patients with EGFR mutations included non-smoker in 20 patients, light smoker (< 10 pack-years smoker) in 4, and heavy smoker (> 10 pack-years smoker) in 14. Multivariate analyses showed that non-smoker or light smoker (p=0.007) and adenocarcinoma (p=0.044) were the significant predictive factors contributing to EGFR mutations. Gender, serum CEA level, and clinical stage were not associated with EGFR mutations. Seventy patients treated with gefitinib and 25 PR were observed, and the overall response rate was 36%. The response rate to gefitinib in patients with and without EGFR mutations were 76% and 7%, respectively. In addition, EGFR mutations were detected in 51% (19/37) of patients with adenocarcinoma and light smoker, and the response rate to gefitinib of them was 49% (18/37). Conclusions: In Japanese patients with lung cancer, non-smoker or light smoker and adenocarcinoma were significant predictive factors for mutations in EGFR exon 19 and 21. No significant financial relationships to disclose.

Effect of Cigarette Smoking on the Critical Flicker Frequency of Heavy and Light Smokers

In order to evaluate the effects of smoking on CFF, heavy and light smoker thresholds were determined 5 min. and 1 min. before, and then 1, 5, 10, and 15 min. after 10 inhalations of a cigarette. Although both groups of smokers showed a significant elevation in CFF immediately after smoking, the light smokers' CFF gradually returned to pre-smoking levels, while the heavy smokers' CFF fell below and then rose above the pre-smoking level.